The purpose of this project was to investigate the influence of hormones, maternal diabetes, and maternal fasting on fetal lung maturation. Maternal diabetes depressed in vitro incorporation of (14C) glucose, palmitate, glycerol, choline into fetal lungs. In another series of experiments maternal rats were fasted the last four days of gestation. Maternal fasting was associated with low fetal plasma levels of insulin, glucose and elevated levels of fetal plasma glucagon, glycerol, and fatty acids. In vitro incorporation of (14C) glucose and palmitate into lung lipids were depressed. These data show that both nutritional alterations and hormonal alterations (maternal diabetes) interfere with carbohydrate and lipid metabolism in the fetal lung at the critical period in lung maturation just prior to birth. In a third series of experiments the influence of placenta hormones on fetal lung cells were examined. The presence of placenta hormones showed a 21% increase in protein content, 30% increase in DNA, 42% increase in lung cell glycogen and a 15% increase in disaturated phosphatidyl (DSPC) choline. The incorporation of 3H-choline into DSPC was increased 36% by placenta treated fetal lung cells. These data show that fetal lung cells are responsive to placenta hormones and that these hormones released from the placenta may play an important role in lung development during the last trimester of gestation.